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Biomedical subjects

M Huie

Publications and source records attributed to M Huie.

8 recordsLinked to original sources
PubMed2000

Frequent mutations in Japanese patients with acid maltase deficiency.

We screened 22 Japanese patients with acid maltase deficiency (seven with the infantile type, eight with the juvenile type and seven with the adult type) for three previously described mutations, D645E, S529V and R672Q, and a novel mutation, R600C. Although D645E has been reported to be common in Chinese patients with the infantile type, only three of 44 alleles (two of 14 infantile type alleles) from Japanese patients harbored the D645E mutation. The S529V mutation was identified in six of 14 alleles from adult-onset patients. None of the infantile or juvenile patients harbored the S529V mutation. Therefore, S529V apparently results in the adult type disease and is common in Japanese adult-onset patients. R672Q was identified in two pairs of siblings with the juvenile type. A novel mutation, R600C, was identified in eight of 22 patients (nine of 44 alleles). Therefore, R600C is another common Japanese mutation occurring at a CpG dinucleotide "hot spot". Homozygosity for this mutation apparently results in the infantile phenotype. Genetic diagnosis by detecting these four mutations might be feasible for most Japanese patients with acid maltase deficiency.

Adolescent↗
PubMed1995

Identification of C1q as the heat-labile serum cofactor required for immune complexes to stimulate endothelial expression of the adhesion molecules E-selectin and intercellular and vascular cell adhesion molecules 1.

To examine the role of complement components as regulators of the expression of endothelial adhesive molecules in response to immune complexes (ICs), we determined whether ICs stimulate both endothelial adhesiveness for leukocytes and expression of E-selectin and intercellular and vascular cell adhesion molecules 1 (ICAM-1 and VCAM-1). We found that ICs [bovine serum albumin (BSA)-anti-BSA] stimulated endothelial cell adhesiveness for added leukocytes in the presence of complement-sufficient normal human serum (NHS) but not in the presence of heat-inactivated serum (HIS) or in tissue culture medium alone. Depletion of complement component C3 or C8 from serum did not prevent enhanced endothelial adhesiveness stimulated by ICs. In contrast, depletion of complement component C1q markedly inhibited IC-stimulated endothelial adhesiveness for leukocytes. When the heat-labile complement component C1q was added to HIS, the capacity of ICs to stimulate endothelial adhesiveness for leukocytes was completely restored. Further evidence for the possible role of C1q in mediating the effect of ICs on endothelial cells was the discovery of the presence of the 100- to 126-kDa C1q-binding protein on the surface of endothelial cells (by cytofluorography) and of message for the 33-kDa C1q receptor in resting endothelial cells (by reverse transcription-PCR). Inhibition of protein synthesis by cycloheximide blocked endothelial adhesiveness for leukocytes stimulated by either interleukin 1 or ICs in the presence of NHS. After stimulation with ICs in the presence of NHS, endothelial cells expressed increased numbers of adhesion molecules (E-selectin, ICAM-1, and VCAM-1). Endothelial expression of adhesion molecules mediated, at least in part, endothelial adhesiveness for leukocytes, since leukocyte adhesion was blocked by monoclonal antibodies directed against E-selectin. These studies show that ICs stimulate endothelial cells to express adhesive proteins for leukocytes in the presence of a heat-labile serum factor. That factor appears to be C1q.

Antigen-Antibody Complex↗
PubMed1985

Inhibition of an IUD-induced precocious luteolysis by prostaglandin E1 (PGE1) in sheep.

Fifteen ewes were assigned as they came into estrus to one of three randomized treatment groups: 1. Sham IUD + Vehicle, 2. IUD + Vehicle or 3. IUD + PGE1 in vehicle. An IUD was inserted adjacent to the luteal-bearing ovary on day 3 postestrus. Prostaglandin E1 (500 micrograms) in vehicle (Na2CO3) or vehicle was given intrauterine through an indwelling uterine cannula every four hours from day 3 postestrus until ewes returned to estrus. Precocious estrus was induced in both the sham IUD and IUD groups receiving vehicle. Prostaglandin E1 prevented an IUD-induced premature luteolysis based on daily concentrations of progesterone in peripheral blood and the interestrous interval. It is concluded that an IUD-induced premature luteolysis is not necessarily via physical distention by the IUD. It is also concluded that chronic intrauterine infusions of PGE1 can prevent an IUD-induced premature luteolysis.

Alprostadil↗
PubMed1985

Effects of prostaglandin E2 (PGE2) on estradiol-17 beta-induced luteolysis in the nonpregnant ewe.

Fifteen ewes were assigned as they came into estrus to the following randomized treatment groups: 1) Vehicle (1 ml corn oil + vehicle Na2CO3 buffer), 2) Estradiol-17 beta + vehicle and 3) Estradiol-17 beta + PGE2 (500 micrograms) in Na2CO3 buffer (5 ewes/treatment group). Prostaglandin E2 was given through an intrauterine cannula every four hours from days 8 through 15 postestrus. PGE2 prevented a luteolytic dose of estradiol-17 beta given on days 9 and 10 from causing a precocious luteolysis. PGE2 maintained concentrations of progesterone in peripheral blood (days 8 through 15) and weights and concentrations of progesterone in corpora lutea on day 15 postestrus of ewes receiving estradiol-17 beta. It is concluded that chronic intrauterine infusions of PGE2 can prevent an estradiol-17 beta-induced premature luteolysis.

Animals↗
PubMed1985

Effects of prostaglandin E1 (PGE1) on estradiol-17 beta induced luteolysis in the nonpregnant ewe.

Nonpregnant ewes were assigned as they came into estrus to one of the following randomized treatment groups: 1) Vehicle (1 ml corn oil) + Vehicle (buffer), 2) Estradiol-17 beta + Vehicle (buffer) or Estradiol-17 beta + PGE1 in buffer. Ewes were unilaterally ovariectomized on day 8 postestrus and an intrauterine cannula was installed in the uterine horn adjacent to the remaining luteal-bearing ovary. Buffer of PGE 1 (500 micrograms) in buffer was infused intrauterine every 4 hours from day 8 through day 15. Luteolysis was initiated by giving an intramuscular injection of estradiol-17 beta (500 micrograms) on days 9 and 10. Chronic intrauterine infusions of PGE1 maintained jugular progesterone through day 15 and weights of corpora lutea and progesterone in corpora lutea on day 15 although luteolysis was initiated by estradiol. It is concluded that chronic intrauterine infusions of PGE1 can prevent an estrogen-induced premature luteolysis.

Alprostadil↗
PubMed1985

Prostaglandin E2 (PGE2) inhibits an IUD-induced premature luteolysis in sheep.

Fifteen ewes were assigned as they came into estrus to one of three randomized treatment groups: 1. Sham IUD + Vehicle, 2. IUD + Vehicle, and 3. IUD + PGE2 in Vehicle. An IUD was inserted adjacent to the luteal-bearing ovary of unilaterally ovariectomized ewes on day 3 postestrus. Vehicle (Na2CO3) or PGE2 (500 micrograms) in vehicle was given every 4 hours intrauterine through an indwelling uterine cannula from day 3 postestrus until ewes returned to estrus. Luteolysis was advanced in both the Sham IUD and IUD groups receiving vehicle. An IUD-induced premature luteolysis was prevented by PGE based on daily concentrations of progesterone in peripheral blood and the extended interestrous interval. It is concluded that chronic intrauterine injections of PGE2 (500 micrograms) every four hours can prevent an IUD-induced premature luteolysis. It is also concluded that an IUD-induced premature luteolysis is not necessarily through uterine distention.

Animals↗
PubMedDate not supplied

Procedures provided to Medicaid recipients by pediatric, general and public health dentists in the commonwealth of Virginia: fiscal years 1994 and 1995.

PURPOSE: The purpose of this study was to report any differences found among the mean percentages of procedures performed by three types of dental providers for each type of service performed. The study focused on the types of services provided by dentists to Medicaid children in Virginia. METHODS: Medicaid claims field for dental patients younger than age 21 were obtained and analyzed for fiscal years 1994 and 1995. Dental providers were categorized according to their practice: general practice (GP), pediatric dentist (PD) and public health dentist (PH). Each type of practitioner (GP, PD, and PH) was evaluated for percentages of diagnostic, preventive, and corrective services provided to their Medicaid patients. The preventive category was subdivided into preventive services (scaling, prophy, fluoride and oral hygiene instruction) and sealant services. RESULTS: For each type of service, the mean percentages of procedures performed were compared among the three types of dental providers. The evaluation of the diagnostic procedure variable resulted in the finding that GP practitioners performed a significantly greater percentage of diagnostic procedures to their Medicaid patients than do PD and PH dentists (p < 0.0001). The percentage of preventive procedures performed by PD and GP dentists was not significantly different but was significantly lower than those performed by PH dentists (p < 0.0001). Finally, PD dentists performed a significantly greater percentage of corrective procedures than both GP and PH dentists (p > 0.0037). CONCLUSION: Differences were found among the mean percentages of procedures performed by the three types of dental providers for each type of service performed.

Adolescent↗